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Updated: Aug 8, 2026

Isolation and Flow Cytometric Analysis of Glioma-infiltrating Peripheral Blood Mononuclear Cells
Published on: November 28, 2015
Identification and characterization of an anti-tyrosine kinase factor in cystic gliomas
F Berger1, M Laine, G Amalfitano
1INSERM U. 318, CHU Grenoble, France.
Abstract:
In view of the frequent activation of the epidermal growth factor receptor (EGF-R) in gliomas and autocrine hypothesis, we searched for 'EGF-like' factor(s) in cystic fluids (CFs) associated with gliomas. Membranes of A431 cells, which overexpress EGF-R, were used to explore such activity in 20 CFs. In all cases CFs induced inhibition of EGF-R phosphorylation. Biochemical analysis revealed an anti-tyrosine kinase activity which was identified as a 18 kDa proteic factor. Effectiveness at high dilution and anti-proliferative effect on living cells in culture suggest that this factor may be involved in the negative regulation of glial oncogenesis.
Insights
Researchers discovered an 18 kDa protein in glioma cystic fluids that inhibits epidermal growth factor receptor (EGF-R) phosphorylation. This anti-tyrosine kinase factor shows potential for negative regulation of glial oncogenesis.
Area of Science:
- Oncology
- Biochemistry
- Cell Biology
Background:
- Epidermal growth factor receptor (EGF-R) is frequently activated in gliomas.
- The autocrine hypothesis suggests self-stimulation in tumor growth.
- Glioma cystic fluids (CFs) were investigated for potential regulatory factors.
Purpose of the Study:
- To identify EGF-like factors in glioma CFs.
- To investigate the effect of CFs on EGF-R activity.
- To characterize the biochemical nature of inhibitory factors.
Main Methods:
- Utilized A431 cell membranes overexpressing EGF-R to test CFs.
- Performed biochemical analysis to identify the active component.
- Assessed anti-proliferative effects on cultured cells.
Main Results:
- All tested CFs inhibited EGF-R phosphorylation.
- An 18 kDa proteic factor with anti-tyrosine kinase activity was identified.
- The factor demonstrated effectiveness at high dilution and anti-proliferative effects.
Conclusions:
- A novel 18 kDa inhibitory factor exists in glioma CFs.
- This factor may play a role in the negative regulation of glial oncogenesis.
- Further research is warranted to explore therapeutic potential.

